ORIGINAL ARTICLE

Abnormal Ankle Brachial Index and the Presence of Significant

Coronary Artery Disease
Fuad Hakeem, Saulat Siddique and Qazi A. Saboor

ABSTRACT
Objective: To determine the association between an abnormal ankle brachial index (ABI) and the presence of significant
coronary artery disease (CAD) on coronary angiography.
Study Design: Cross-sectional, observational study.
Place and Duration of Study: The study was carried out at Sheikh Zayed Hospital, Lahore, from July to October 2007.
Methodology: A series of 41 patients undergoing coronary angiography in Sheikh Zayed Hospital were selected and their
ABI were calculated before the diagnostic coronary angiography. ABI calculations and coronary angiography reporting
were done by separate individuals and data was analysed using SPSS 12.0. All patients undergoing diagnostic coronary
angiography were included in the study except for those having peripheral arterial disease documented by lower extremity
revascularization, lower extremity ulceration and lower extremity amputation. Proportion were compared using chi-square
test with significance at p < 0.05.
Results: Out of the 41 patients 31 male (76%) and 10 female (24%), 3 patients (7.31%) had ABI < 0.9 and all 3 had triple
vessel disease. Ten patients (24%) had ABI 0.91-0.99 and 2 (20%) of them had single vessel disease. Two (20%) had
double vessel disease and 6 (60%) had triple vessel disease. Twenty four patients (58%) had ABI of 1.00-1.28 and 8 (33%)
of these had single vessel disease, 3 (12%) had double vessel disease and 13 (55%) had triple vessel disease, while 4
patients had normal coronaries. A total of 22 patients were found to have triple vessel disease and only 3 (13.6%) of these
22 patients had an ABI < 0.9 which is statistically not significant (p=0.07).
Conclusion: This study was not able to establish a direct association between ABI and significant CAD as only 3 patients
out of 22 with triple vessel disease had an ABI < 0.9. However, an approximately log linear relationship was noted between
ABI and CAD risk which means that not only the average CAD risk increased exponentially at values < 1.0 but also that
the CAD risk continued to decline as ABI values increased above 1.0.

Key words: ABI (Ankle brachial index). CAD (Coronary artery disease). Risk association. Coronary angiography.

INTRODUCTION disease (CAD) and myocardial infarction (MI) still occurs

Ischemic heart disease (IHD) is the major cause of
morbidity and mortality all over the world.1 It is usually
attributable to atherosclerotic obstruction of coronary
vessels and clinically presents as a spectrum of signs
and symptoms ranging from angina pectoris to acute
myocardial infarction (AMI), more aptly termed as acute
coronary syndrome.2 The age adjusted incidence of
AMI, the most life threatening form of IHD, is 192/1000
in the male population and 19/1000 in the female
population of Pakistan.3 A number of risk factors are
known to predispose patients to IHD. Some of these
cannot be modified, for example age, gender and family
history. Modifiable risk factors include dyslipidemia,
hypertension, smoking, diabetes mellitus, obesity,
physical inactivity, alcohol consumption and psycholo-
gical factors.4 These conventional risk factors do not
account for all cases of atherosclerotic coronary artery
Department of Cardiology, Sheikh Zayed Hospital, Lohare.
Correspondence: Dr. Fuad Hakeem, 19-H2, Johar Town,
Lahore.
E-mail: fuadhakeem@yahoo.com
Received June 19, 2008; accepted September 26, 2009.
in individuals having no obvious traditional risk factor.
These observations under-score the need to identify
additional risk factors for coronary atherosclerosis.
The presence of peripheral arterial disease measured
non-invasively by ankle brachial index (ABI) is a risk
marker for coronary artery disease (CAD) and a
predictor of coronary events in the elderly.5-7 However,
the relevance and application of the ABI as a screening
test for patients at risk for CAD remains unclear. The
ankle brachial index (ABI), a ratio of ankle systolic blood
pressure to brachial systolic pressure, is used in clinical
practice to assess the patency of the lower extremity
arterial system and to screen for the presence of
occlusive peripheral arterial disease. Epidemiological
and clinical studies have found that low ABI levels are
associated with cardiovascular risk factors, coronary
and carotid artery disease and predict cardiovascular
and overall mortality.8 The conventional cut off point for
an abnormal ABI i.e. 0.9, was developed from studies of
patients referred for angiography of lower extremities.9-11
The objective of this study was to determine the
association between an abnormal ankle brachial index
(ABI) and the presence of significant coronary artery
disease (CAD) on coronary angiography.

Journal of the College of Physicians and Surgeons Pakistan 2010, Vol. 20 (2): 79-82 79
Fuad Hakeem, Saulat Siddique and Qazi A. Saboor

METHODOLOGY hypercholesterolemics were defined as patients having

total cholesterol > 200 mg/dl. The results were obtained
Patients referred for diagnostic cardiac catheterization
using SPSS version 12, p-value was calculated by chi-
were enrolled from July to October 2007 at Sheikh
square test and p < .05 was considered as significant.
Zayed Hospital, Lahore, after informed consent. All
patients had ankle and arm blood pressures recorded
using a blood pressure cuff and a hand-held-Doppler. RESULTS
The ankle brachial index (ratio of the ankle/highest The baseline risk factors for coronary artery disease
brachial systolic pressure) was calculated before were diabeties in 20 (49%), hypertension in 22 (54%),
cardiac catheterization. After resting for 5 minutes in a smoking in 12 (29%), hypercholesterolemia in 6 (15%)
supine position, brachial artery systolic and diastolic and positive family history of IHD in 22 (54%).
blood pressure was recorded in both arms using a
Out of 41 patients, there were 31 male (76%) and 10
mercury sphygmomanometer. Appropriate sized blood
female (24%). Three patients (7.31%) had ABI < 0.9 and
pressure cuffs were applied over each brachial artery.
all 3 had triple vessel disease. Ten patients (24%) had
The cuff was rapidly inflated to 20 mmHg above the
ABI of 0.91-0.99, 2 (20%) of them had single vessel
audible systolic pressure in each arm and then deflated
disease, 2 (20%) had double vessel disease and 6
at a rate of 2 mm per heart beat to the lowest even
(60%) had triple vessel disease. Twenty four patients
reading. Highest systolic reading was measured in both
(58%) had ABI 1.00-1.28, 8(33%) of them had single
arms as the pressure at which the first sustained sound
vessel disease, 3 (12%) had double vessel disease and
was audible. Diastolic pressure was recorded at the
13 (55%) had triple vessel disease, while 4 patients had
disappearance [phase five] of Korotkoff sounds. The
normal coronaries.
higher of the two arms’ pressure was taken as index
arm. Two more readings were taken on the same arm In the studied population, a total of 22 patients were
and the average was taken as the index systolic blood found to have triple vessel disease and only 3 (13.6%)
pressure in the arm. of those 22 patients had ABI < 0.9 which was statistically
not significant (p=0.07). Direct inverse relationship was
In all cases, ankle pressure in both ankles was
not established between significant CAD and ABI as
measured by Doppler with 8 MHz probe which is the
only 3 patients out of 22 patients with triple vessel
Gold standard. The cuff was positioned on the ankle
disease had ABI < 0.9. However, an approximately log
proximal to the malleoli. The pulse was located with a
linear relationship was noted between CAD risk and ABI
Doppler probe and the cuff inflated until the pulse was
which means that not only the average CAD risk
obliterated; the cuff was deflated and the pressure was
increased exponentially at values < 1.0 but also that the
recorded at the point when the pulse reappeared. The
CAD risk continued to decline as ABI values increased
leg with lower systolic pressures was taken as index leg.
above 1.0 (Figure 1).
Within the index leg, dorsalis pedis artery pressure was
taken as index ankle pressure if it was higher than the
posterior tibial and vice versa. Two more readings were
taken on the same artery and the average was
recorded.
ABI (ankle brachial index) was calculated by dividing the
average systolic blood pressure of the index ankle artery
by the average systolic blood pressure of the index arm.
Patients underwent diagnostic coronary angiography.
Single vessel CAD was defined as > 50% stenosis by
qualitative coronary analysis in a major coronary artery
i.e. left anterior descending artery (LAD), left circumflex
(LCx) or right coronary artery (RCA). CAD in the
diagonal or marginal vessels was also classified as
single vessel CAD. Double vessel CAD was defined as
> 50% stenosis in two major coronary arteries. Severe Figure 1: Log-linear association between an abdominal ABI and CAD risk.
triple vessel CAD was defined as the presence of CAD
in the left main stem or > 3 vessel CAD. Diabetics were
defined as patients having either previously diagnosed DISCUSSION
diabetes mellitus or having abnormal fasting blood Ankle brachial index (ABI) is a good predictor of
glucose levels (> 110 mg/dl) on three consecutive peripheral artery disease, stroke and cardiovascular
occasions. Hypertensives were defined as patients events in the middle aged and older population.12 ABI
having blood pressure > 140/90 mm Hg (JNC VII) and was used in these patients to assess its relationship with

80 Journal of the College of Physicians and Surgeons Pakistan 2010, Vol. 20 (2): 79-82
Abnormal ankle brachial index and the presence of significant coronary artery disease
the presence of significant coronary artery disease as
an abdominal AB was hypothesized to be associated
with significant coronary artery disease. In the studied
population, a direct inverse relationship was not
established between ABI and coronary artery disease.
The observed difference may be due to the fact that very
strong exclusion criteria were used and no patient in the
studied population had documented peripheral artery
disease. Western studies have shown that the African
American populations have a substantially higher
prevalence of peripheral artery disease (PAD) and
borderline ABI than non African American populations.13-18
Other possible reasons could be a smaller sample size
and short study duration. Moreover, there were marked
proportions who lacked important risk factors such as
smoking, hypertension and diabetes.
However, an approximately log linear association was
noted between ABI and CAD risk. This means that not
only the average CAD risk increased exponentially at
values < 1.0 but that CAD risk continued to decline as
ABI values increased above 1.0. In this study, all 3
patients who had ABI < 0.9 had triple vessel disease.
Out of the 10 patients with ABI, 0.91-0.99 6 (60%) had
triple vessel disease. Out of the 24 patients with ABI
1.00-1.29, 13 (55%) had triple vessel disease. This
again confirms the log-linear association between an
abdominal ABI and CAD risk.
Data from ARIC (Atherosclerosis Risk In Communities)
and other studies suggest that the average risk of future
coronary heart disease (CHD) events increases with
decreasing ABI as a continuous but not linear function.
Similar results have been reported for exertional leg
pain, for carotid intima media thickness and coronary
artery calcium.19 The choice of relevant ABI cut off at
which risk factor modification therapy should be
instituted to reduce further CAD risk should be based on
absolute rather than relative risk of future CAD events.
This requires further long-scale studies with better
controlled risk factors and a larger sample size to attain
adequate study power.
This study established a log-linear relationship between
ABI and CAD risk as it showed that not only the average
CAD risk increased exponentially at values < 1.0 but that
the CAD risk continued to decline as ABI values
increased above 1.0. It is not clear, however, how much
additional information ABI can provide as a non-invasive
screening tool above and beyond that provided by
traditional risk factors at cut-off values that can guide
clinical practice.
CONCLUSION
This study was not able to establish a direct association
between ABI and significant CAD as only 3 patients out
of 22 with triple vessel disease had an ABI < 0.9.
However, an approximately log-linear relationship was
Journal of the College of Physicians and Surgeons Pakistan 2010, Vol. 20 (2): 79-82
noted between ABI and CAD risk which means that not
only the average CAD risk increased exponentially at
values < 1.0 but also that the CAD risk continued to
decline as ABI values increased above 1.0.
REFERENCES
1. Robert C, Leslie D, Killian R, Eileen N, Brain F. Hyper-
homocysteinemia: an independent risk factor for vascular
disease. N Engl J Med 1991; 324:1149-55.
2. Antman EM, Braunwald E. Acute myocardial infarction. In:
Braunwald E, editor. Heart disease: a text book of cardio-
vascular medicine. 7th ed. Philadelphia: W.B.Saunders 2005:
1184-1270.
3. Samad A, Sehibzada WA, Nazir F, Khan AA. Incidence of acute
myocardial infarction. Pak J Cardiol 1996; 1:14-7.
4. Ross R. The pathogenesis of atherosclerosis. In: Braunwald E,
editors. Heart disease: a textbook of cardiovascular medicine.
5th ed. Philadelphia: W. B. Saunders; 1997. p. 1105-25.
5. Aronow WS, Ahn C. Prevalence of co-existence of coronary
artery disease, peripheral arterial disease and atherothrombotic
brain infarction in men and women > or =62 years of age. Am J
Cardiol 1994; 74:64-5.
6. McDermott MM, Liu K, Guralnik JM, Mehta S, Criqui MH,
Martin GJ, et al. The ankle brachial index independently predicts
walking velocity and walking endurance in peripheral arterial
disease. J Am Geriatr Soc 1998; 46:1355-62.
7. Hirsch AT, Criqui MH, Treat-Jacobson D, Regensteiner JG,
Creager MA, Olin JW, et al. Peripheral arterial disease detection,
awareness and treatment in primary care. JAMA 2001; 286:
1317-24. Comment in: p. 1380-1.
8. Newman AB, Shemanski L, Manolio TA, Cushman M, Mittlemark
M, Polack JF, et al. Ankle-arm index as a predictor of
cardiovascular disease and mortality in the cardiovascular
health study. The cardiovascular health study group. Arterioscler
Thromb Vasc Biol 1999; 19:538-45.
9. Zheng ZJ, Sharrett AR, Chambless LE, Rosamond WD, Nieto
FJ, Sheps DS, et al. Association of ankle-brachial index with
clinical coronary heart disease, stroke and pre-clinical carotid
and popliteal atherosclerosis: the atherosclerosis risk in
communities (ARIC) study. Athersclerosis 1997; 131:115-25.
10. Murabito JM, Evans JC, Larson MG, Nieto K, Levy D, Wilson
PW. Framingham study. The ankle-brachial index in the elderly
and risk of stroke, coronary disease and death: the Framingham
study. Arch Intern Med 2003; 163:1939-42.
11. Murabito JM, Evans JC, Nieto K, Larson MG, Levy D, Wilson
PW. Prevalence and clinical correlates of peripheral arterial
disease in the Framingham offspring study. Am Heart J 2002;
143:961-5.
12. Grundy SM, Howard B, Smith S, Eckel R, Redberg R, Bonow
RO. Prevention conference VI. Diabetes and cardivoascular
disease: executive summary. Conference proceeding of
healthcare professionals from a special writing group of the
American Heart Association. Circulation 2002; 105:2231-9.
13. Van der Meer IM, Bots ML, Hofman A, del Sol AI, van der Kuip
DA, Witteman JC. Predictive value of non-invasive measures of
atherosclerosis for incident myocardial infarction: the Rotterdam
study. Circulation 2004; 109:1089-94. Epub 2004 Mar 1.
81
Fuad Hakeem, Saulat Siddique and Qazi A. Saboor
14. Aronow WS. Prevalence of atherothrombotic brain infarction,
coronary artery disease and peripheral arterial disease in
elderly blacks, Hispanics and Whites. Am J Cardiol 1992; 70:
1212-3.
15. Newman AB, Siscovick DS, Manolio TA, Polak J, Fried LP,
Borhani NO, et al. Ankle-arm index as a marker of
atherosclerosis in the cardiovascular health study. Cardio-
vascular Heart Study (CHS) collaborative research group.
Circulation 1993; 88:837-45.
16. Kullo IJ, Bailey KR, Kardia SL, Mosley TH Jr, Boerwinkle E,
Turner ST. Ethnic differences in peripheral arterial disease in the
NHLBI Genetic Epidemiology Network of Arteriopathy (GENOA)
study. Vasc Med 2003; 8:237-42.
● ● ● ● ●
82
17. Selvin E, Erlinger TP. Prevalence of and risk factors for
peripheral arterial disease in the United States: results from the
National Health and Nutrition Examination Survey, 1999-2000.
Circulation 2004; 110:738-43. Epub 2004 Jul 19.
18. McDermott MM, Liu K, Criqui MH, Ruth K, Goff D, Saad MF,
et al. Ankle-brachial index and subclinical cardiac and carotid
disease: the multi-ethnic study of atherosclerosis. Am J Epidemiol
2005; 162:33-41.
19. Wang JC, Criqui MH, Denenberg JO, McDermott MM, Golomb
BA, Fronek A. Exertional leg pain in patients with and without
peripheral arterial disease. Circulation 2005; 112:3501-8.
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Journal of the College of Physicians and Surgeons Pakistan 2010, Vol. 20 (2): 79-82